What Are Hypercoagulable States?

Hypercoagulable state means that patients with nephrotic syndrome have increased anti-aggregation, anticoagulation and fibrinolytic mechanisms due to the increase of pro-aggregation and coagulation factors in the blood, as well as venous stasis, hyperlipidemia, hypoproteinemia, Blood concentration, increased blood viscosity, the use of hormones and diuretics, etc. cause the increase of plasma fibrinogen levels and the significant increase in the content of fibrin and fibrinogen degradation products, which ultimately lead to more protein C and protein S levels Normal or increased, but its activity is reduced, resulting in a hypercoagulable state. Anticoagulant drugs can be used clinically to improve this state.

Hypercoagulable state

Hypercoagulable state means that patients with nephrotic syndrome have increased anti-aggregation, anticoagulation and fibrinolytic mechanisms due to the increase of pro-aggregation and coagulation factors in the blood, as well as venous stasis, hyperlipidemia, hypoproteinemia, Blood concentration, increased blood viscosity, the use of hormones and diuretics, etc. cause the increase of plasma fibrinogen levels and the significant increase in the content of fibrin and fibrinogen degradation products, which ultimately lead to more protein C and protein S levels Normal or increased, but its activity is reduced, resulting in a hypercoagulable state. Anticoagulant drugs can be used clinically to improve this state.

Causes of hypercoagulability

Patients with nephrotic syndrome are prone to hypercoagulability for a number of reasons, including increased aggregation and procoagulant factors in blood, and impaired anti-aggregation, anticoagulation, and fibrinolytic mechanisms, as well as venous stasis, hyperlipidemia, low Proteinemia, blood concentration, increased blood viscosity, use of hormones and diuretics. The most direct evidence of the hypercoagulable state of nephrotic syndrome is an increase in plasma fibrinogen levels. The rate of plasma fibrinogen catabolism is normal in patients with nephrotic syndrome, and the increase in plasma fibrinogen level is due to its increased synthesis.

In addition, fibrin and fibrinogen degradation products also increased significantly. Plasma fibrinogen and metabolic disorders can disappear with the recovery of nephrotic syndrome. Coagulation factors V, IX, IX, X are also elevated, which may be related to increased liver synthesis. Increased platelet aggregation is also one of the reasons for the hypercoagulable state of nephrotic syndrome, which may be related to hypoalbuminemia, hyperlipidemia, and a decrease in the sialic acid glycoprotein content of the platelet membrane to prevent platelet aggregation. Abnormal fibrinolytic and anticoagulant systems include decreased plasminogen levels (although increased levels of plasminogen activator), increased a2-macroglobulin, and decreased antithrombin III (loss from urine). Anti-plasmin, anti-trypsin a1 plasminogen activating factor, and endothelial prostacyclin-stimulating factor were also reduced.

In nephrotic syndrome, protein C and protein S levels are usually normal or increased, but their activity decreases, resulting in a hypercoagulable state.

Prevention of hypercoagulability

Patients with nephrotic syndrome are in a hypercoagulable state due to changes in coagulation factors, especially when the plasma albumin is below 20-25 g / L, which may cause venous thrombosis. Clinically used anticoagulants are:

(1) Heparin: mainly by activating antithrombin III (ATIII) activity. The usual dose is 50 75mg / d by intravenous drip, which makes the AT vitality unit above 90%. There are reports in the literature that heparin can reduce proteinuria and improve renal function in nephrotic syndrome, but its mechanism of action is unclear. It is worth noting that heparin (MW65600) can cause platelet aggregation. There are still small molecular weight heparin subcutaneous injections, once a day.

(2) Urokinase (UK): directly activates plasminogen, leading to fibrinolysis. The commonly used dose is 20,000 to 80,000 U / d, starting from a small dose, and can be intravenously dripped with heparin at the same time. Monitor the euglobulin dissolution time to make it between 90 and 120 minutes. The main side effects of UK are allergies and bleeding.

(3) Warfarin: Inhibit the synthesis of vitamin K-dependent factors , , X, and X in liver cells. The commonly used dose is 2.5 mg / d orally, and the prothrombin time is monitored to make it 50% to 70% of normal people. .

(4) Pansentin: a platelet antagonist, commonly used at a dose of 100-200mg / d. The general anticoagulation time in the hypercoagulable state is 2 to 8 weeks, and then it is changed to warfarin or pansentin. Those with venous thrombosis: The thrombus is removed surgically. Interventional thrombolysis. Intravenous radiation is injected into the renal artery at a rate of 240000 U to dissolve renal venous thrombosis. This method can be repeated. systemic intravenous anticoagulation. That is, heparin plus urokinase, the course of treatment is 2 to 3 months. Oral warfarin to remission of nephrotic syndrome to prevent thrombosis. ^[1]